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Maternal Programming of Defensive Responses 149expression and conclude with the questions that remain to be answered in regardto the effects of early stress on pathology.The Role of Early Life StressEpidemiological studies reveal the importance of family function and early lifeevents as predictors of mental health in adulthood (Repetti et al., 2002). Such studiesshow that the quality of family life influences the development of individualdifferences in vulnerability to illness throughout life. Importantly, such effectsinclude vulnerability for obesity, metabolic disorders, and heart disease, as wellas affective disorders and drug abuse (e.g., Feletti et al., 1998; Lissau & Sorenson,1994; McCauley et al., 1997). Recent findings from epidemiological studies (e.g.,Caspi et al., 2003), as well as from primate models (e.g., Bennett et al., 2002),further suggest that developmentally determined vulnerability can emerge fromthe interaction between genotype and early environmental events, including earlylife adversity. In each of these studies, the consequences associated with a geneticvariant (the short variant of the serotonin transporter promoter) were defined bythe quality of parent–offspring interactions. As exemplified in these wonderfulstudies, the critical questions for developmentalists concern the identity of therelevant genomic targets, the nature of the gene–environment interactions and theirrelation to specific phenotypic outcomes.Such studies have fueled a renewed interest among neuroscientists in theeffects of early environment on neural development and emotional/cognitivefunction. From the basic sciences, “stress diathesis” models have emerged asexplanations for the effects of early life on health in adulthood and suggest thatadversity in early life alters the development of neural systems in a manner thatpredisposes individuals to disease in adulthood. These models place considerableemphasis on the influence of early experience on the development of defensiveresponses and the relevance of these effects for vulnerability over thelife span. Chronic illness is thought to emerge as a function of the altered responsesto environmental demand (stressors) in conjunction with an increasedlevel of prevailing adversity.There are two critical assumptions here: first, that prolonged activation of neuraland hormonal responses to stressors can promote illness, and second, that earlyenvironmental events influence the development of stress responses. There isstrong evidence in favor of both ideas. In humans, physical and/or sexual abusein early life, poor parental bonding, and family dysfunction increase endocrineand autonomic responses to stress in adulthood and adolescence (de Bellis et al.,1994; Essex et al., 2002; Heim et al., 2000, 2002; Luecken & Lemery, 2004;Pruessner et al., 2004), as well as dysfunctional cognitive processing of potentiallythreatening stimuli.